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PubMedDate not supplied

Peripheral nerve injury and repair.

Peripheral nerve injuries are common, and there is no easily available formula for successful treatment. Incomplete injuries are most frequent. Seddon classified nerve injuries into three categories: neurapraxia, axonotmesis, and neurotmesis. After complete axonal transection, the neuron undergoes a number of degenerative processes, followed by attempts at regeneration. A distal growth cone seeks out connections with the degenerated distal fiber. The current surgical standard is epineurial repair with nylon suture. To span gaps that primary repair cannot bridge without excessive tension, nerve-cable interfascicular auto-grafts are employed. Unfortunately, results of nerve repair to date have been no better than fair, with only 50% of patients regaining useful function. There is much ongoing research regarding pharmacologic agents, immune system modulators, enhancing factors, and entubulation chambers. Clinically applicable developments from these investigations will continue to improve the results of treatment of nerve injuries.

Humans↗
PubMed2005

Promoting neurological recovery following a traumatic peripheral nerve injury.

If a peripheral nerve is crushed, or if the nerve is cut and the ends sutured together soon after the lesion (anastomosed), neurological recovery is good. When a length of a peripheral nerve is destroyed, and anastomosis is not possible, the standard surgical repair technique is to graft a length/s of sensory nerve from the patient, into the gap. For gaps <2 cm neurological recovery is moderate, for gaps 2-4 cm recovery is generally poor, and for gaps >4 cm recovery is limited to non-existent. The limited recovery is because sensory nerves act as passive scaffolds for axon regeneration and do not actively promote axon regeneration. However, such grafts remain the "gold standard" for nerve repairs. New techniques are required that induce improved neurological recovery. This paper reviews current clinical and basic research techniques for inducing neurological recovery following traumatic peripheral nerve injuries.

Humans↗
PubMed1980

Clinical and experimental aspects of injection injuries of peripheral nerves.

Injury to peripheral nerves complicating deep intramuscular injections of antibiotic and other agents is well recognized and can result in significant permanent neurological deficit. The purpose of this paper is to review the subject of nerve injection injuries, and report on a series of recent experimental studies carried out in this laboratory designed to improve our understanding of the pathophysiology of this condition and help provide a rational basis for its treatment. A wide variety of chemotherapeutic, prophylactic, and local anaesthetic agents in common use were injected into the sciatic nerve of the adult Wistar rat. Both intrafascicular and extrafascicular injections were examined. Results revealed that the site of injection was the most crucial factor in determining the degree of nerve fiber injury. Following intrafascicular injection, the degree of injury varied significantly, depending upon the specific agent injected. The most severe injuries were associated with wide-spread axonal and myelin degeneration. Pathological alterations in the nerve were evident as early as 30 minutes following injection injury. Regeneration was a constant finding in nerve damage by injection of the various agents. The mechanism of injury appeared to be a direct toxic effect of the injected compound on neural tissue, with an associated break down of the blood-nerve barrier.

Anesthetics, Local↗
PubMed1997

Endogenous NGF and CNTF levels in human peripheral nerve injury.

Nerve growth factor (NGF) is trophic to sensory and sympathetic fibres, and ciliary neurotrophic factor (CNTF) to motoneurones, in animal models of peripheral nerve injury: NGF excess produces hyperalgesia. In this first study of injured human nerves and sensory ganglia, we quantified and localized endogenous NGF and CNTF in 59 neonate and adult patients with brachial plexus and peripheral nerve injury. NGF levels were generally depleted in injured nerves, but relatively preserved acutely in nerve segments distal to injury. NGF immunostaining was observed in Schwann cells in distal nerve segments with pockets of high levels in some neuromas. CNTF levels and immunostaining in Schwann cells were markedly decreased distally within days of injury. We propose that early local administration of NGF and CNTF-like agents may help prevent degenerative changes in injured nerves, while at later stages local anti-NGF treatment (e.g. of some neuromas) may ameliorate chronic pain.

Adolescent↗
PubMed1992

Pathobiological reactions of C-fibre primary sensory neurones to peripheral nerve injury.

Mammalian primary sensory neurones display profound anatomical and chemical changes in response to injury of their peripheral processes. Peripheral nerve damage results in transganglionic degeneration of central terminals of A-fibre primary afferent neurones terminating in the deeper layers of the medullary or spinal dorsal horn. The depletion of neuropeptides and other neurone-specific macromolecules from neurones in sensory ganglia and from the superficial dorsal horn, the known central projection area of C-fibre primary afferents, is a salient phenomenon commencing after peripheral nerve lesions. A recently devised new experimental procedure, termed the capsaicin-gap method, permitted evaluation of the transganglionic degenerative phenomena which develop in C-fibre primary sensory neurones after a lesion is inflicted upon their peripheral branches. The experimental findings indicated that C-fibre primary afferent terminals underwent transganglionic degeneration following a perineural treatment with capsaicin, and that this was associated with, and probably resulted from, ganglionic cell degeneration. Studies on the effects of peripheral nerve section yielded similar results. It has therefore been suggested that the observed depletion of specific macromolecules, including sensory peptides, specific glycoconjugates and sensory neurone specific acid phosphatase, may be accounted for, at least in part, by an irreversible loss of sensory ganglion neurones. In contrast, many injured neurones express peptides, including vasoactive intestinal polypeptide, peptide histidine-isoleucine and galanin, which can be demonstrated in only a few neurones under normal conditions. These seem to be involved in dorsal horn regenerative and/or compensatory processes following peripheral nerve damage. There is suggestive evidence that the partial deafferentation caused by the transganglionic degeneration of C-fibre primary afferents creates favourable circumstances for an anatomical rearrangement of neuronal connections within the spinal cord dorsal horn. These changes may provide a morphological substrate of some of the functional alterations demonstrated after peripheral nerve lesions.

Animals↗
PubMed1984

The repair of peripheral nerve injuries in emergency.

Peripheral nerve injuries must be considered as serious surgical emergencies for they are often associated with vascular lesions. Primary repair of clean-cut injuries of peripheral nerves by microsurgical techniques yields better results than the best of secondary repairs.

Electromyography↗
PubMed1996

Sprouting of sympathetic nerve fibers into the dorsal root ganglion following peripheral nerve injury depends on the injury site.

Peripheral nerve injury often induces sympathetic nerve fiber sprouting in the dorsal root ganglion (DRG) and injured nerve. Presently, the underlying mechanism and functional significance of the sprouting are unknown. This study was performed to see whether the degree of the sprouting in the DRG was a function of the distance between the DRG and injury site. To this aim, we compared two groups of rats with respect to the sympathetic nerve fibers sprouting in the S1-3 DRG; one group was subjected to unilateral inferior and superior caudal trunk transections at the level between the S3 and S4 spinal nerves (S34 group) and the other group at the levels between the S1 and S2, between S2 and S3 and between S3 and S4 spinal nerves (S123 group). The transections in both groups equally eliminated the inputs from the tail to the S1-3 DRG, but the distance from the S1/S2 DRG to the injury site was different between the two groups. Immunohistochemical staining with tyrosine hydroxylase (TH) antibody of the S1-3 DRG removed from rats a week after the injury revealed that the degree of penetration of TH-positive fibers into the S1 and S2 DRG was much more extensive in the S123 group than in the S34 group, whereas that into the S3 DRG was not significantly different between the two groups. These results suggest that the extent of the sympathetic nerve fiber sprouting in the DRG following peripheral nerve injury is inversely related to the distance between the DRG and injury site.

Animals↗
PubMed1988

Changes in the central projection pattern of vibrissae innervating primary sensory neurons after peripheral nerve injury in the rat.

The central representation of a normal vibrissa nerve and the corresponding nerve after transection and regeneration of the infraorbital nerve has been studied by the use of transganglionic transport of horseradish peroxidase in the adult rat. The normal vibrissa nerve terminated in a well-defined area within nucleus caudalis and C1 dorsal horn. In contrast, the regenerated vibrissa nerve showed a widespread central termination pattern indicating a pronounced loss of somatotopic organization. These changes in somatotopic organization could contribute to an inability to correctly localize a sensory stimulus; this is a common clinical finding after peripheral nerve injury and regeneration.

Animals↗
PubMed2000

BDNF is involved in sympathetic sprouting in the dorsal root ganglia following peripheral nerve injury in rats.

Peripheral nerve injury results in sympathetic sprouting around large diameter sensory neurons in the dorsal root ganglia (DRG). The mechanism underlying this pathological phenomenon is not known. Brain-derived neurotrophic factor (BDNF) is up-regulated in large sensory neurons and ensheathing satellite cells following a sciatic nerve injury. In the present study, we investigated the effects of BDNF on the sympathetic sprouting in the DRG, by delivering BDNF antibody or antisense oligodeoxynucleotide to injured DRGs, or by delivering exogenous BDNF to intact DRGs. The sheep antibody to BDNF, characterized by bioassays and dot blots, specifically reacted with BDNF but not other neurotrophins. Noradrenergic fibers were visualized by immunostaining of tyrosine hydroxylase (TH) and quantified by an NIH Imaging program. Two weeks following L5 spinal nerve lesion, a dramatic increase in TH-immunoreactive (-ir) fibres was observed in both ipsi- and contralateral DRGs in normal sheep IgG treated rats. BDNF antibody significantly reduced the sprouting of sympathetic nerves in both ipsi- and contra-lateral DRGs by 67% and 42% respectively. BDNF antisense oligodeoxynucleotide, by inhibiting BDNF synthesis in DRGs, also significantly suppressed the sprouting by 67% and 60% respectively in the ipsi- and contra-lateral DRGs. Delivery of exogenous BDNF into an intact L5 DRGs resulted in an increase in the sprouting by 4.2-fold. Our results clearly indicate that BDNF, synthesized in and secreted from the DRGs, is involved in the sympathetic sprouting in the DRG following the peripheral nerve injury.

Journal Article↗
PubMed1982

Peripheral nerve injuries. Nerve sutures and nerve grafting.

In the repair of transected peripheral nerves it is attempted to achieve an optimal coaptation of the fascicular tissue. A certain amount of fibroblast activity is essential for nerve regeneration but the fibroblast activity should not be overwhelming. At present fibroblast activity can be reduced only -by resection of the epineural tissue in nerve segments, in which it represents a high percentage of the cross-section (polyfascicular nerve structure with group arrangement), -by reducing the surgical trauma to a minimum, -by reducing the application of foreign material to a minimum, -by avoiding tension at the suture site, -by performing a proper resection, and -by adjusting the type of coaptation to the structure prevailing in the two nerve stumps. In clean cuts without major complications primary nerve repair is recommended. The patients have to be followed and, if within six months no signs of recovery occur, re-exploration is indicated. Complicated cases with nerve defects should be treated by early secondary repair. If during secondary repair an end-to-end coaptation can not be achieved easily, the application of nerve grafts is the treatment of choice.

Axons↗
PubMed2003

Free radical-induced damage in experimental peripheral nerve injection injury.

Peripheral nerve injury secondary to injection of therapeutic agents is well-documented. Until recently, the precise mechanism of injury has been obscure; even today, the treatment of these nerve injection injuries remains controversial. The aim of this study was to determine the involvement of ischemia-reperfusion injury in the development of peripheral nerve injection injury. Wistar rats were randomized into three groups. Sciatic nerve was used as the standardized nerve injection injury model. Two commonly used agents, lidocaine HCl 1 percent and phenol 5 percent, were tested for their comparative effects on the sciatic nerve. Lidocaine and phenol were injected into the sciatic nerves of the rats in Groups 1 and 2, respectively. Physiologic saline was used in the controls (Group 3). All the agents were injected intrafascicularly. The effects of nerve injection injury were assessed by measuring thiobarbituric acid reactive substance (TBARS) levels and obtaining walking-track analyses (WTA). Nerve injection caused significant increases in TBARS levels, which were correlated with the severity of the injury. The TBARS levels were related to the severity of injury caused by the tested agents; TBARS levels in phenol-injected nerves were significantly higher than those of lidocaine-injected nerves. Patterns of alterations in TBARS levels also paralleled the changes in print-length factor. Injection of lidocaine and phenol resulted in near-normal walking tracks at 8 and 12 weeks, respectively, while saline injection caused only transient impairment in walking tracks. These findings indicate that reactive oxygen species are involved in the pathogenesis of experimental peripheral nerve injection injury. Indices of free oxygen radical damage correlate with the progression of functional alterations after nerve injection injury.

Analysis of Variance↗
PubMedDate not supplied

[Microsurgical reconstruction of peripheral nerve injuries].

The results of peripheral nerve repair have been significantly improved since introduction of the operating microscope. Microsurgical repair enables better fascicular orientation and coaptation with diminished fibrotic reaction on the suture line. The ten-year experience in 421 patients with peripheral nerve injuries is analyzed in the paper. Different surgical procedures (interfascicular neurolysis, direct fascicular repair, interfascicular transplantation or brachial plexus reinnervation) have been performed depending on type of injury, the special attention is paid to the cases with the nerve transection and consecutive interfascicular grafting. The results are analyzed in 182 cases depending on the location of injury, the patient's age, the timing of surgery and the length of nerve grafts.

Adolescent↗
PubMed1999

Peripheral nerve injuries secondary to missiles.

Peripheral nerve injuries secondary to missiles can present some of the most challenging problems faced by hand surgeons. This article reviews the pertinent neural anatomy, injury classifications, and repair techniques. Options in the management of nerve gaps are presented including the use of vascularized nerve grafts. The results are discussed and a treatment algorithm is presented.

Algorithms↗